Emergencies in Cardiac Intensive Care - PowerPoint Presentation

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Emergencies in Cardiac Intensive Care

Doda Sarridou MD PhD EDAIC AFICM PGD

Christos

Chamos

MD EDAIC AFICM

Simon Liu BSc FRCA FFICM

Stuart McCorkell FRCA FFICM

Martin John

BSc MBBS MRCP FRCA

Department of Cardiac

Anaesthesia

and OIR

Guy’s and St Thomas’ NHS Foundation Trust

Hot topics in OIR

Haemorrhage

post Cardiac Surgery

Tamponade

post Cardiac Surgery

Management of inotropes and vasopressors

Temporary Pacing

CALS protocol

Bleeding

First steps

Control systolic pressures – target 90-120mmHg depending on co- morbidities e.g.

cerebro

-vascular disease. Use GTN (1

st

line) /Labetalol (2

nd

line) infusion to control BP

Target

Hb

>85g/L

Keep patients sedated and ventilated to avoid straining and in case of surgical re-exploration

Avoid excessive IV fluids (colloid, crystalloid) when correcting hypovolaemia - they can create or worsen

dilutional

coagulopathy.

Use blood products when available to treat active bleeding.

Consider placing patients in Trendelenburg position and starting low dose noradrenaline infusion as required until blood products are available.

Check cross matched PRBC are available in the theatre fridge/blood bank, ensure you have 4.

Investigations and treatment

Send ICU profile bloods ASAP and repeat regularly (FBC, coagulation studies, U+Es)

Target fibrinogen > 2.0 using cryoprecipitate 2 pools for adults

Normalise INR and

APTTr

using FFP.)

Correct residual Heparin effect (Check ACT or compare

APTTr

vs INR -Protamine 25-50mg IV)

Give tranexamic acid 2g IV

Give Platelets if patient has received recent antiplatelet therapy

Coagulopathy - the fatal triad of hypothermia, hypocalcaemia and acidosis

Actively rewarm – monitor temperature and aim for

normothermia

Bair hugger

IV fluid warmer –

vital

for PRBC stored at 4℃

Check Calcium (either via U+Es or ABGs). Titrate Calcium Chloride 10% IV 3-5mg boluses slow push

Correct any respiratory component of acidosis

Haemorrhage Part I

Teamwork – Surgical/ Blood bank / Haematology

Inform surgical team (0200) and consultant covering OIR

Significant bleeding may need surgical re-exploration

As a guide – blood loss of >3ml/kg 1st hour, >2ml/kg 2nd hr, >1ml/kg any subsequent hr is excessive

Initiate ‘Code Red’ if catastrophic bleeding – call 2222 announce ‘Code Red’ and location. Switch will have the lab call back immediately and send a porter to lab to collect blood/products ASAP

Useful numbers (Blood bank 84774 Bleep 0201 Haematology

Reg

0122 in hours, via switch out of hours)

Tamponade post Cardiac Surgery

Diagnosis:

It is ultimately clinical and needs a high index of suspicion!

You must think of it as a differential in a deteriorating cardiac surgical patient in order to diagnose it

Is based on:

signs of low cardiac output: hypotension/

escalating doses of vasopressors

/ oliguria/ poor peripheral perfusion/ rising lactate AND

echocardiographic evidence of pericardial fluid or clots +/- echo signs of tamponade (cardiac chamber collapse/ variation in blood flow through cardiac valves)

Remember TTE gives poor views postop and cannot exclude a posterior pericardial effusion

Beck’s triad (

high central venous pressure (CVP) or distended neck veins/ hypotension/ reduced cardiac sounds)

is not always present.

Hypovolaemia, beta blockade, pacing, noisy environment can mask diagnostic signs. Similar to other subtle signs (electrical

alterans

- ECG/

pulsus

paradoxus

)

Typically chest drainage will be reduced or absent (often following increased drain output)

First presentation can be arrhythmia or cardiac arrest.

For hypotension and rising inotrope requirement: Main differential diagnosis post cardiac surgery is ventricular dysfunction. Echocardiography will distinguish between the two conditions.

Tamponade Post Cardiac Surgery

Urgent surgical re-exploration.

Pericardiocentesis

in almost never an option in cardiac surgical patients

Usually performed in East wing cardiac theatres. But may have to take place in OIR / ITU in the case of an extremely unstable patient.

Immediately inform: cardiac surgical registrar (bleep 0200) and consultant cardiac anaesthetist

Out of hours you may have to transfer patient to theatres until senior anaesthetist arrives.

In the meantime:

Try to maintain normal

haemodynamics

and CO: fluid and/ or blood administration, vasopressors and/or inotropes. The patient will need high systemic vascular resistance, high normal heart rate, preservation of sinus rhythm if possible.

Keep patient sedated + paralysed in view of re-exploration

Correct any coagulopathy/ order appropriate blood products

Inotropes and Vasopressors

-Commonly used agents on OIR

Noradrenaline ( 0.01-0.20 mcg/kg/min)

Dobutamine

( 1-10 mcg/kg/min)

Milrinone

( 0.01-0.3 mcg/kg/min)

Hypotension will be manifested with acute drop on the BP, tachycardia +/-, rise of the CVP and is associated with high requirements of vasopressors and inotropes.

-Causes of Hypotension

:

-

Hypovolaemia

, (surgical Bleeding output > 400mls/h, or > 200

mls

first 2-3 hours. Coagulopathy ( Needs PLT, FFP,

Cryo

)

tamponade

( presence of blood or clots in the pericardium, normally low drain

ouput

, CVP>20)

pump failure ( acute or acute on chronic LV/RV failure)

inflammatory response to surgery (long CPB time)

-Correct hypothermia, consider Heparin rebound effect repeat ACT

-Management out of hours

acute deterioration



Always inform the consultant on call

Communicate the concern with the rest of the team , Nurse in charge , other SPRs

Do not escalate NAD more than 0.2 mcg/kg/min - Initiate CO monitoring , ( PICCO, LIDCO, Normal CO >4-5, CI> 2). CV gas> 70%

Inform 0200 usually- experienced trainees and senior fellows

Consider TOE ( OIR cons) or TTE, call 0100 cardiology SPR

Temporary Pacing

What’s the first rule?

You need to differentiate the heart’s response to pacing from the ECG appearance. The arterial line or

oximetry

trace will show you when the heart is contracting, the ECG will show you pacing spikes.

Why do cardiac patients need temporary pacemakers?

>3% of cardiac patients require pacing in postoperative period most commonly for AV block,

bradycardia

or to improve cardiac output with sequential AV pacing.

Pre-existing conduction defect, Diabetes, valve surgery, high

cardioplegia

volumes and pacing required to separate from bypass are the major predictors of pacing requirement postoperatively.

Epicardial

pacing wires reduce risk from low CO state or heart block but bring new risks of infection, myocardial damage, perforation and TAMPONADE - especially on removal.

Risk/benefit ratios vary between patients so there is no universally accepted practice. At GSTT the majority of patients who receive

cardioplegia

have RV wires implanted, some may have RA wires in addition. LA and LV wires are rare.

Temporary Pacing

How do we check a pacemaker’s function?

Initial check is done in theatre on setting up pacing and thresholds should be confirmed in handover.

It is checked once daily by the nursing staff during the day shift when immediate expert help is present. You are not expected to do this but must understand the process.

DO NOT interrupt pacing if patient is dependent on it – seek consultant advice.

Check

UNDERLYING RHYTHM

– turn rate down until patient’s rhythm is exposed, record native ECG. See below for rate setting.

Check

SENSITIVITY

– the minimum voltage the pacemaker can sense.

If patient has no underlying rhythm to detect, set sensing voltage to 2mV.

If patient has an underlying rhythm:

Turn pacing rate below patient’s native rate.

Increase voltage setting (less sensitive) until sensing light stops flashing with each native QRS complex. Pacing spikes will appear on ECG.

Reduce voltage setting (more sensitive) until sensing light flashes with each native QRS, this is the pacing threshold.

Set to half this threshold.

Check

CAPTURE

– the minimum output that will stimulate an action potential in the patient’s heart.

DO NOT CHECK capture threshold if there is no underlying rhythm – you may not regain capture once lost.

Set pacing rate above native rate, minimum 80. Confirm every pacing spike is followed by a QRS. If not, you are already below capture threshold.

Reduce pacing voltage until capture is lost.

Increase voltage until capture is regained - this is the capture threshold.

Set voltage to 2V above capture threshold and confirm reliable capture is restored.

Troubleshooting

Failure to pace

Heart rate is lower than rate set on pacemaker and there are no pacing spikes on ECG.

Causes

Battery in pacemaker has

failed

Lead

or connector

malfunction

Sensitivity

voltage set too low – pacemaker is inhibited by electrical interference (patient movement,

equipment)

Pacemaker

inhibited by ectopic activity with too small a voltage to show on surface

ECG

Cross-talk

inhibition (dual chamber systems only)

Resolution

Check battery indicator on pacemaker and change pacemaker if failed

Switch temporarily to fixed rate mode (V00, D00). If there are still no visible pacing spikes, 3-5 are eliminated as cause.

If indicated above, check connections (wear gloves), change connector lead, change pacemaker.

INFORM CONSULTANT

Temporary Pacing

Failure to capture

There are pacing spikes on ECG but no mechanical association – the arterial or

oximetry

waveform does not correspond with the pacing rate.

Causes

Increased resistance at electrode tip, usually inflammatory fibrosis

Hyperkalaemia, profound acidosis

Drugs e.g. Beta blockers, sodium channel blockers, calcium channel blockers

Resolution

Increase output voltage until capture returns

Swap connector around to reverse polarity (wear gloves)

Correct metabolic and drug causes

Put backup method of pacing in place ASAP as the wire is likely to fail in time – external pacing via defibrillator or

transvenous

pacing via cardiology registrar

INFORM CONSULTANT- External Pacing via

Defibrilator

CALS Algorithm

CALS approach

Most cardiac patients in OIR will have full invasive and

capnography

monitoring.

-Arrest is confirmed by a flat arterial line trace, central venous pressure and pulse

oximetry

, as well as a reduced

capnography

trace.

No need to reassess for 10 seconds and the first responder should immediately initiate the arrest protocol (attached to arrest trolley),

inform the cardiothoracic surgeons (bleep 0200) and call for the

resternotomy

trolley.

The priority is to immediately manage the arresting rhythm and open the chest (within 5 mins).

Managing the arresting rhythm

i

)

VF /VT

External chest compressions can be delayed for no more than

1 minute

to allow for expeditious defibrillation.

Deliver

3 sequential defibrillation attempts at 150J.

If unsuccessful, immediate chest opening is advised. External cardiac compression should also be commenced (compression depth target = 60 mmHg on art line trace at a rate of 100

bpm

).

Amiodarone

300mg

(bolus)

should be administered via the central line and one further defibrillation attempt at 150J should be made every

2

mins

until the chest is opened.

ii)

Asystole

/severe

bradycardia

Disruption of intrinsic cardiac conduction is common post operatively and patients may have single chamber (ventricular), dual chamber (atrial and ventricular) or no pacemaker system attached. External cardiac compressions can be delayed for no more than

1 minute

to allow for establishing pacing.

Single chamber systems

: Ensure the pacing wires are connected to a functioning pacing box. Set stimulation thresholds to maximum (15V, full anticlockwise turn). Set pacing rate to 80-100

bpm

. Asynchronous pacing is appropriate (Set sensing dial at

asynch

, full clockwise turn).

Look for pacing spike capture on

ecg

.

Dual chamber systems:

Ensure the pacing wires are connected to a functioning pacing box. Set stimulation thresholds (Both Atrial [A] and Ventricular [V]) to maximum. Set rate at 80-100

bpm

. Set pacing mode to

DDD.

(Alternatively, some boxes have an emergency button which activates appropriate asynchronous pacing which can be pressed).

Look for pacing spike capture on

ecg

.

No pacing system:

Start external cardiac massage whilst setting up for attempted external cardiac pacing (maximum threshold at a rate of 80-100

bpm

). If external pacing fails, the chest needs reopening.

iii)

Pulseless electrical activity

This rhythm is non

shockable

and not amenable to pacing so external cardiac compressions as well as plans for

resternotomy

should be commenced immediately.

Note; If a

paced

patient develops PEA, then the pacemaker should first be turned off to rule out underlying VF.

Airway management

Increase Fio2 to 100% and confirm ET position + cuff inflation. Listen for breath sounds to exclude

pneumo

/

haemothorax

.

Drugs

Following arrest, stop all infusions (many cause vasodilatation).

If awareness is a concern, sedative infusions can be continued at the discretion of the senior clinician.

Adrenaline

(particularly at conventional arrest doses) can precipitate catastrophic harm so do not give unless a senior doctor advises this.

Atropine

for

asystole

or extreme

bradycardia

is not recommended.

Summary

All the above conditions are life threatening and require immediate senior response and input

INFORM CONSULTANT ON CALL

Correct Coagulopathy if any

Correct

hypovolaemia

Call 0200 – Cardiac Surgery SPR/Fellow

Call 0100 – Cardiology SPR

Consider TTE or TOE